ROLE OF CARDIOVASCULAR STRESS IN THE PATHOGENESIS OF ENDOCARDITIS AND GLOMERULONEPHRITIS: Observations Including Method of Experimental Production Utilizing Arteriovenous Fistulas

THE OBSERVATION1 has been made that dogs with large arteriovenous fistula loads "spontaneously" acquired endocarditis and that in some acute proliferative glomerulonephritis also developed in the period of six weeks to five months following the construction of their arteriovenous shunts. The mechanism of these observations would appear to depend on the fact that the application of a systemic cardiovascular stress, such as large arteriovenous fistulas, causes certain physiological alterations to occur within the dogs, which result in a significant and specific increase in the susceptibility of the endothelial surfaces of the heart and kidneys to bacteria or to the products of bacterial infection. This increase in susceptibility is so great that the animals can acquire their endocarditis from the relatively few microorganisms which gain entrance into their blood streams by adventitious routes. This fortuitous entrance of bacteria through skin or intestinal mucosal abrasions into the blood stream no doubt